Term
| What are the 4 major obstructive lung diseases? |
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Definition
All involve increased resistance to expiratory airflow.
COPD and Asthma most common
1) COPD
2) Asthma
3) Bronchiectasis
4) Bronchitis |
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Term
| What histological features define Chronic bronchitis? |
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Definition
Productive cough >3 months each year for 2 years
**Often seen with Emphysema in chronic obstructive pulmonary disease**
1) Airway inflammation and edema
2) Mucous gland hypertrophy
3) Excessive secretions |
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Term
| What histological features define Emphysema? |
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Definition
Predominantly affects pulmonary parenchyma
1) Destruction of alveolar walls leading to airspace enlargement
2) Destruction of pulmonary capillary bed |
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Term
| What alterations to respiratory mechanics occur in Emphysema? |
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Definition
1) Increased Airway resistance
- loss of normal "tethering" effect of pulmonary parenchyma on small, non-cartilaginous airways leading to collapse when exposed to positive pressures during exhalation.
2) Decreased recoil
- Destruction of collagen and elastin fibers decreases elastic recoil, causing decrease in expiratory flow rate |
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Term
| How are lungs volumes altered in Emphysema? |
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Definition
Decreased elastic recoil
1) FRC increases
2) Increased TLC (if muscle strength is maintained)
3) "air trapping" by collapsed airways can increase RV and decrease in VC
4) ERV increases because time available for expiration is insufficient to allow system to return to EQ ("Dynamic hyperinflation") |
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Term
| What is "Dynamic Hyperinflation" and how does it relate to Emphysema? |
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Definition
1) ERV increases because time available for expiration is insufficient to allow the system to return to equilibrium
2) Elastic recoil pressure therefore remains positive (intrinsic PEEP), and can contribute to further compression and collapse. |
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Term
| How is Gas exchange altered in obstructive lung disease? |
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Definition
1) Increased numbers of low V/Q lung units cause a decrease in PaO2 and an increase in the PA-aO2.
2) High V/Q units lead to an increase in alveolar and physiologic dead space. |
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Term
| Why do you see exercise-induced hypoxemia in patients with moderate to severe emphysema, but not other obstructive lung diseases? |
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Definition
Only emphysema causes destruction of pulmonary capillaries.
CO increases and a huge amount of blood is going very quickly through a reduced # of capillaries, reducing equilibration time with alveoli. PaO2 falls as a result. |
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Term
| Why can acute CO2 retention occur with accompanying oxygen administration in chronic obstructive disease? |
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Definition
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Term
| How is Respiratory Muscle function altered in obstructive lung disease? |
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Definition
1) Increased work leads to high energy consumption
2) Diaphragm loses dome-shape, leading to reduced efficiency
3) Intrinsic PEEP acts as a threshold load on respiratory muscles and further increases energy expenditure (you can't start to inspire until you correct the expiration!) |
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Term
| What would a pulmonary function test of a patient with Emphysema (or any obstructive lung disease) look like? |
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Definition
FVC N - ↓
FEV1 ↓
FEV1/FVC ↓
PEFR ↓
FEF25-75 ↓
FRC N - ↑
RV N - ↑
TLC N - ↑
DLCO N - ↓ |
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Term
| What long-term pathophysiologic changes take place in chronic obstructive lung disease? |
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Definition
1) Pulmonary HTN
**Worsened by hypoxia-induced erythrocythemia (increased blood viscosity).
2) Capillary destruction and hypoxia-induced vasoconstriction lead to decrease in cross-sectional area and increase in PVR.
3) Intimal thickening
4) Pulm HTN can lead to RHF ("cor pulmonale") with increased JVP, hepatomegaly and peripheral edema. |
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Term
| Why do you see dyspnea and exercise limitation in obstructive lung disease? |
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Definition
1) Increased airway resistance produces dynamic hyperinflation, which limits RR, increases muscle load and decreases Vt maximum falls
2) Respiratory muscle fatigue along with increased Vd/Vt (due to decreased Vt) produce dyspnea.
ALSO: Arterial hypoxemia, excessive alveolar dead space (which increases ventilation requirements), and increased work and energy expenditure by the respiratory muscles. |
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Term
| How does emphysema, in particular, produce dyspnea and exercise limitation? |
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Definition
1) Alveolar/capillary destruction produces V/Q inequality;Diffusion impairment.
2) Decreased PaO2 and increased Vd produce dyspnea
**Increased airway resistance also reduces Vt and increases muscle load (producing fatigue and increasing Vd/Vt) like in all other obstructive pulmonary diseases** |
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Term
| What gross and histological changes do you see in Chronic bronchitis? |
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Definition
Remember, this is chronic cough ad sputum production for most days for 3 months out of year for 2 years.
1) Gross
- Extensive mucus plugging of air passages, associated with boggy, edematous and erythematous bronchial mucosa with bronchial pits (dilated ducts of mucus secreting glands).
2) Histology
- Goblet cell hyperplasia and squamous metaplasia of columnar epithelium
- Hypertrophy/hyperplasia of tracheobronchial mucus glands
- Inflammatory (acute and chronic) infiltrate with in submucosa and BM thickening
- Goblet cell metaplasia in TBL accompanied by bronchiolitis |
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Term
| What gross and histological changes do you see in Emphysema? |
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Definition
COPD manifested as abnormal permanent enlargement of airspaces distal to terminal bronchioles, due to destruction of alveolar walls.
1) Gross
- voluminous and frequently in context of barrel chest deformity, with extension of lungs across midline of anterior mediastinum
- Apical bullae may be apparent (air-filled balloons)
2) Histologically
- Centrilobular (smoking in upper lobes at RB:duct junction)
- Panacinar (Diffuse involvement of alveolar ducts in lower lobes in patients with alpha-1-anti-trypsin deficiency)
- Localized/Periseptal (adjacent to scars/fibrosis in distal portions of acinus at apex, progressing to bulla)
- Irregular (irregular involvement of acinus associated with scaring) |
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Term
| What is the "protease-anti-protease" Theory of emphysema? |
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Definition
Normally, there is a protease (elastase): anti-protease (alpha-1-anti-tyrpsin) balance, which keeps elastic tissue of lung intact.
1) When patient smokes, PMNs infiltrate pulmonary parenchyma, leading to activation of elastase.
2) Elastase activity is now higher than a1-anti-trypsin activity, and there is destruction of elastic tissue in distal alveolar septa (walls)
3) Decrease in elastic tissue is responsible for decreased expiratory volume, because of decreased elastic recoil on expiration. |
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Term
| What are the 4 major histological forms of Emphysema and their important characteristics? |
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Definition
1) Centrilobular
- upper lobes at RB:duct junction of smokers
2) Panacinar
- Diffuse involvement of alveolar ducts in lower lobes in patients with alpha-1-anti-trypsin deficiency
3) Localized/Periseptal
- adjacent to scars/fibrosis in distal portions of acinus at apex, ultimately progressing to bulla
4) Irregular
- irregular involvement of acinus (as opposed to peri-septal which is distal)
- associated with scaring |
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Term
| What gross and histological changes do you see in Asthma? |
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Definition
Tracheobronchial reactivity and smooth muscle constriction
1) Gross
- lungs distended with air
- segmental and sub-segmental bronci are plugged with mucus
2) Histologically
a) Epithelial hyperplasia with goblet cell metaplasia and hypertrophy/hyperplasia of tracheobronchial glands (Eosinophils and Charcot-Leyden crystals of eosinophils)
b) BM thickening
c) Submucosal infiltrates of eosinophils and lymphocytes
d) Hypertrophy and hyperplasia of bronchial smooth muscle wall from prolonged constriction |
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Term
| What are Curshmann's spirals and Charcot-Leyden crystals and what disease are they seen in? |
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Definition
Histologically in Asthma
1) Curshmann's spirals are seen on cytology and are spirals of inspissated mucus of tracheobronchial glands
2) Charcot-Laeydon crystals are coalesced eosinophil membrane protein crystaloids seen in mucus plugs. |
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Term
| What are 2 important complications associated with Asthma? |
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Definition
1) Saprophytic fungal infection
2) Bronchopneumonia |
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Term
| What are the 3 major causes of Bronchiectasis? |
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Definition
Irreversible dilation of bronchi as a result of destruction of muscular and elastic components of bronchial wall.
1) Bronchial obstruction
2) Post-inflammatory dilation (most common)
- Example is TB
3) Congenital
- Example is Kartageners |
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Term
| What gross and histological changes do you see in Bronchiectasis? |
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Definition
1) Gross
- Mucus plugging of tracheobronchial tree
- Affects Lower lobe
- Saccular (proximal without continuation of airway, which becomes fibrotic and collapsed)
- Cylindrical (6th-8th branching with uniform moderate dilation)
- Varicose (irregular dilations and constriction)
2) Histologically
- Similar to chronic bronchitis with squamous metaplasia of epithelium and submucosal inflammation.
- Extensive scarring of parenchyma
- Hyperplastic and enlarged bronchial arteries in submucosa (Hemoptysis) |
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Term
| What are the 3 major types of Bronchiectasis? |
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Definition
1) Saccular
- proximal without continuation of airway, which becomes fibrotic and collapsed
2) Cylindrical
- 6th-8th branching with uniform moderate dilation
- Long, tubular toothpaste enlargements
3) Varicose
- irregular dilations and constriction |
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Term
| What gross and histological changes do you see in CF? |
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Definition
1) Gross
- Normal at birth, but in 1st month you see mucus plugging, bronchitis and bronchopnuemonia
- Over-inflated with scattered areas of collapse or fibrosis and bronchiectasis
- Pneumothorax common in adults
2) Histologically
- Distended bronchioles and bronchi with inspissated mucus
- Squamous metaplasia of bronchial lining epithelium.
- PMNs in walls
- Pneumonia and focal fibrosis of peripheral lungs |
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